Chen Zhenhua,Ren Chunmei,Wan Rensheng,Pan Yue,Wu Qiuxiang,Yuan Shuangxue,Wang Dongxu,Huang Jun,He Baicheng,Sun Wenjuan.Correlation of PI3K/Akt signaling pathway with anti-proliferative effect of evodiamine in colon cancer cells[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(05):492-495.
Chen Zhenhua,Ren Chunmei,Wan Rensheng,Pan Yue,Wu Qiuxiang,Yuan Shuangxue,Wang Dongxu,Huang Jun,He Baicheng,Sun Wenjuan.Correlation of PI3K/Akt signaling pathway with anti-proliferative effect of evodiamine in colon cancer cells[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(05):492-495.DOI:
Correlation of PI3K/Akt signaling pathway with anti-proliferative effect of evodiamine in colon cancer cells
Objective To determine the anti-proliferative effect of evodiamine (Evo) on colon cancer cells and investigate the possible underlying mechanism. Methods LoVo cells were treated with 0
0.5
1
2 and 4 μmol/L Evo
and then the anti-proliferation effect of Evo was assessed by crystal violet staining. Flow cytometry was used to determine the apoptosis of LoVo cells after the treatment of 0
0.5
1 and 2 μmol/L Evo. Western blotting was adopted to detect the expression of proliferating cell nuclear antigen (PCNA) and Caspase-3 in the cells treated with 0
0.5 and 1 μmol/L Evo. Hypoxia inducible factor 1-alpha (HIF-α)-responsive firefly luciferase reporter was employed to measure the transcription activity of HIF-1α in 0
0.5
1 and 2 μmol/L Evo treated cells
and Western blotting was used to detect the expression of HIF-1α
Akt1/2
and p-Akt1/2 in the LoVo cells. Results Evo obviously inhibited the proliferation of LoVo cells
down-regulated the expression of PCNA and promoted the cell apoptosis. Luciferase reporter system indicated that Evo decreased the transcriptional activity of HIF-1α in a dose-dependent manner (Evo 0.5 μmol/L
P0.05; 1 or 2 μmol/L
P0.01). Western blotting showed that the expression levels of HIF-1α and p-Akt1/2 were reduced after Evo treatment. Conclusion Evo inhibits the proliferation and promotes the apoptosis in LoVo cells
which may be due to its down-regulating HIF-1α and inhibiting the transconduction of PI3K/Akt signaling pathway.
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Related Author
刘旭
李小丽
周端方
陈波
宋燚
何起臣
于晓萍
曾鸿芳
Related Institution
College of Life Sciences, Beijing University of Chinese Medicine
Hunan Provincial Key Laboratory of Vascular Biology and Translational Medicine, Hunan University of Chinese Medicine
Department of Burn Wounds and Plastic Surgery, First Affiliated Hospital of Hunan University of Chinese Medicine
Department of Neurology Children’s Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics
Department of Thoracic Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University